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Renal Final > Renal Control of Acid-Base Balance > Flashcards

Renal Control of Acid-Base Balance Flashcards

1
Q

Why must pH stay at 7.4?

A
  • some AA have net positive charge or net negative charge at this ph
  • any changes will impact electrostatic charge needed for proper protein folding, alters protein -protein interaction, drug binding/ability to enter cells, etc
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2
Q

Which metabolic acid sources are used for volatile purposes?

- where in body

A

Glucose + O2 -> H+ + HCO3-

Fat + O2 -> H+ + HCO3-

in Lungs (24,000 mEq/ day)

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3
Q

Which metabolic acid sources are used for fixed (nonvolatile) purposes?
- where in body

A

Glucose (anaerobic) -> H+ + lactate

Cysteine + O2 -> H+ + sulfate

Phosphoprotein + O2-> H+ + phosphate

kidneys
(50 mEq/day)

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4
Q

Meaning of Pk

A

pH at which this buffer, acting as “H+ sponge” has sopped up half of the H+ it can hold

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5
Q

Ph of gastric HCl

A

0.8

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6
Q

HCO3-/ H2CO3

  • name buffer system
  • pK value
  • Reaction equation
A

bicarbonate

6.1

H+ + HCO3- <=> H2O + CO2

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7
Q

Hb-/ HHb

  • name buffer system
  • pK value
  • Reaction equation
A

hemoglobin

7.3

HHb <=> H+ + Hb-

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8
Q

HPO4/ H2PO4

  • name buffer system
  • pK value
  • Reaction equation
A

Phosphate

6.8

H2PO4 <=> H + HPO4-

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9
Q

Pr-/ HPr

  • name buffer system
  • pK value
  • Reaction equation
A

plasma proteins

6.7

HPr <=> H+ + Pr-

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10
Q

Four buffer pairs in body buffer system

- what is their rates

A

1) HCO3/ H2CO3
2) Hb-/ HHb
3) HPO4/ H2PO4
4) Pr-/ HPr

ALL instantaneous

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11
Q

Organs in Body Buffer System (4)

- list mechanism

A

1) Lungs
- regulates retention/ elimination of CO2 and H2CO3
2) Ionic Shifts
- exchange of intracellular K and Na for hydrogen
3) Kidneys
- bicarbonate reabsorption/regeneration, ammonia formation, phosphate buffering
4) Bone
- exchange of calcium, phosphate, release of carbonate

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12
Q

Buffering of Hydrogen Ion by Plasma Proteins and Hemoglobin

  • how does H+ enter body for buffering?
  • transport
A

CO2 enter tissues

3 ways of CO2 breakdown in RBC:

a) CO2 dissolved
b) CO2 + H2O <=> H2CO3 <=> HCO3- + H+
c) CO2 + Protein -NH2 <=> Protein + H+

HCO3- + H+
- will use HCO3-/Cl- transport to bring Cl- in , HCO3- out of RBC

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13
Q

Volume of K in ICF? ECF

A 
ICF= 140 mM k+
ECF= 4.0 mM K+
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14
Q

If ECF is in acidemia, what will happen in ICF?

A

ICF takes in H+
= low ECF pH ( <7.35)
= high H+, buffered by raising ECF K+

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15
Q

If ECF is in alkalemia, what will happen in ICF?

A

ICF donates H+
= high ECF pH (>7.45)
= low H, buffered by lowering ECF K

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16
Q

Henderson-Hasselbalch Equation

- which part of equation is controlled by kidneys? lungs?

A

ph= 6.1 + Log [HCO3-]/ [H2CO3]

or

ph= 6.1 + Log [HCO3-]/ (0.03 x PCO2)

[HCO3-]= controlled by kidneys, slow with large capacity

[H2CO3]= controlled by lungs, fast with limited capacity

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17
Q

Ventilatory Rate effect on pH

- hyperventilation? hypoventilation?

A

Hyperventilation= less CO2= less H2Co3= less H= high pH

Hypoventilation= more CO2= more H2Co3= more H= low pH

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18
Q

Renal Reabsorption of Bicarbonate (%)

  • PT
  • Thick LOH
  • CD
A

in Glomerulus : 4320 mEq/ Day

  • PT: 85% , 3672 mEq/ day
  • Thick LOH: 10%, 432 mEq/day
  • CD: 4.9%, 215 mEq/day
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19
Q

Detailed Reabsorption of filtered bicarbonate by Proximal Tubule

  • transports on apical side
  • transports on basolateral side
A

Apical side

  • Na/H exchange ( Na in , H+ out of tubular fluid)
  • H ATPase
  • Bicarbonate -> H2O + Co2 enter cell via carbonic anahydrase

Basolateral side

  • Na/K Atpas
  • Na/ HCo3- co transport (out)
  • HCO3-/ Cl- ( HCO3 out into blood)
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20
Q

What factors increase H+ secretion?

  • Primary (2) / location
  • Secondary (5)/ location
A

Primary (entire nephron)

1) decrease plasma HCO3- (decrease pH)
2) Increase in partial pressure at arterial carbon dioxide

Secondary (all are in PT except #4 is CD)

1) increased in HCO3- filtered load
2) decrease ECF volume
3) increase Ang II
4) increase aldosterone
5) Hypokalemia

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21
Q

What increased during hypokalemia?

why?
- what transporters are involved?

A

ammonia genesis and net acid secretion increased

  • intracellular acidifcation
  • hormones upregulates ammoniagenesis genes to increase NH4+ excretion and decrease K+ secretion
  • renal glutamin transporter SN1
  • mitochondrial glutaminase (GA)
  • glutamate dehydrogenase (GDH)
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22
Q

What factors decrease H+ secretion?

  • Primary (2) / location
  • Secondary (5)/ location
  • when is hyperkalemia relevant
A

Primary (entire nephron)

1) increase plasma HCO3- (increase pH)
2) decrease in partial pressure at arterial carbon dioxide

Secondary (all are in PT except #3 is CD)

1) decreased in HCO3- filtered load
2) increase ECF volume
3) decrease aldosterone
4) Hyperkalemia
- during type IV renal tubular acidosis

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23
Q

Phosphate buffering of secreted hydrogen ions

  • what transports are on apical side?
  • what transports are on basolateral side?
  • what is pathway for Na
A
  • regenerates the plasma HCO3- that had been “consumed” elsewhere when NaH2PO4 lost an H= in acid body
  • H+ into urine

Basolater side

  • Na/K ATPase
  • passive diffusion for HCO3 and CO2

Apical side
- Na/H exchange ( H out into tubular lumen)

NaHPo4- (from tubular lumen) -> NaHPo4 + H+ -> NaH2PO4 -> carries H into the lumen

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24
Q

How ammonia in nephron generate new Bicarbonate

  • in proximal tubule
  • in collecting duct

significance

A

PT
- Glutamine in lumen-> breakdown to ammonia (x2) -> NH3 goes out into tubular fluid -> combine with H+ -> form NH4

-NH3 reabsorbs in tubular fluid

CD
- CO2 + H2O -> H2CO3 via CA-> breaks down into HCO3 + H

HCO3 -> reabsorbs into blood
H+ ->enters tubular fluid into CD

H+ combines with NH3 to become NH4 and excreted into urine

  • uses Na/K/2CL transporter
    NH4 replaces K in this transporter
  • diffuses into CD where it is ion trapped
25
Q

Reabsorption and secretion of bicarbonate in Alpha intercalated cells

  • transporter on apical side
  • transporter on basolateral side
  • significance
A
  • secretes H
  • Reabsorbs HCO3-

apical side

  • K/H ATPase ( K in )
  • H ATPase ( H out)

basolateral membrane
- HCO3/ Cl- antiporter (HCO3 in)

  • “new” bicarbonate is generated during process of urinary acidification when secreted H+ is buffered by NH3-> NH4+, phosphate for excretion while bicarbonate is reabsorbed
26
Q

Reabsorption and secretion of bicarbonate in Beta intercalated cells

  • transporter on apical side
  • transporter on basolateral side
A
  • reabsorbs H+
  • secretes HCO3-

Apical Side
- HCO3/ Cl- antiporter (HCO3 in tubular fluid)

Basal Side
- H+ Atpase ( H into blood)

27
Q

Net Acid Excretion Equaion

- what must it equal?

A

NA= (U(nh4) x V) + (U (Ta) x V) - (U (HCO3) x V)

  • NAE must equal nonvolatile acid production each day in order to maintain acid-base balance
28
Q

Titratable Acids

A

salts of primarily phosphate, sometimes creatinine

~ 1/3 NAE

29
Q

Ammonium ( Nh4+)

A

synthesis and secretion is responsible for ~2/3 NAE

-body can easily make as much as needed

30
Q

Why is ammonium is not measured as about of titratable acidity?

A

high pK of ammonium means no H is removed from NH4 during titration to a ph of 7.4

31
Q

Normal Values of Acid- Base Disturbances

  • ph
  • H+
  • Pco2
  • HCO3-
A

ph= 7.4

H+= 40 mEq/L

PCO2= 40 mmHg

HCo3-= 24 mEq/L

32
Q

Respiratory Acidosis

  • ph
  • H+
  • Pco2
  • HCO3-
A
  • decrease ph
  • increase H+
  • increase Pco2
  • increase HCO3-
33
Q

Respiratory Alkalosis

  • ph
  • H+
  • Pco2
  • HCO3-
A
  • increase ph
  • decrease H+
  • decrease Pco2
  • decrease HCO3-
34
Q

Metabolic Acidosis

  • ph
  • H+
  • Pco2
  • HCO3-
A
  • decrease ph
  • increase H+
  • decrease Pco2
  • decrease HCO3-
35
Q

Metabolic alkalosis

  • ph
  • H+
  • Pco2
  • HCO3-
A
  • increase ph
  • decrease H+
  • increase Pco2
  • increase HCO3-
36
Q

Metabolic Acidosis with compensation and correction

- pathway

A

Renal
low serum ph-> increased acid titration -> increase ammonium and H2PO4-> increase acid excretion in urine-> increase bicarbonate regeneration -> increase serum ph

Respiratory
low serum ph-> hyperventilation-> decrease PCo2-> decrease CO2 + H2O-> decrease H2Co3-> decrease H

37
Q

Normal Anion Gap

A

8-16 mEq/L

38
Q

Causes of Metabolic Acidosis

  • High Anion Gap (9)
  • Non- Anion Gap (7)
A

High Anion Gap (MUDPILERS)

  • Methanol
  • Uremia
  • DKA/ Alcoholic Ketoacidosis
  • Paraldehyde ( obsolete sedative-hypnotic)
  • Isoniazid (used to treat tuberculosis)
  • Lactic Acidosis
  • EtOH/ Ethylene Glycol
  • Rhabdo/ Renal failure
  • Salicylates

Non-Anion Gap (HARDUPS)

  • Hyperalimentation
  • Acetazolamide
  • Renal Tubular Acidosis
  • Diarrhea
  • Uretero-Pelvic Shunt
  • Post-hypocapnia
  • Spironolactone
39
Q

Causes of Metabolic Acidosis (3)

A

1) Excessive production or ingestion of fixed H+
2) loss of HCO3-
- Type 2 renal tubular acidosis ( renal loss of HCO3-)
3) Inability to excrete fixed H
- Type 1 renal tubular acidosis ( decrease excretion of H as titratable acid and NH4)
- Type 4 renal tubular acidosis ( hyperaldosteronism)

40
Q

Type 1 Renal Tubular Acidosis

  • location
  • acidosis?
  • potassium
  • pathophysiology
  • what does it impair
A
  • distal tubules
  • severe acidosis, normal anion gap
  • hypokalemia
  • failure of H+ secretion by alpha intercalated cells
  • impair acid-base homeostasis and phosphate/ammonia buffer
  • urinary stone formation due to hypercalciuria
  • bone demineralization
41
Q

Type 2 Renal Tubular Acidosis

  • location
  • acidosis?
  • potassium
  • pathophysiology
A
  • Proximal Tubules
  • acidosis
  • hypokalemia
  • failed HCO3- reabsorption from urine by proximal tubular cells
42
Q

Type 4 Renal Tubular Acidosis

  • location
  • acidosis?
  • potassium
  • pathophysiology
A
  • adrenal
  • mild acidosis with normal anion gap
  • hyperkalemia
  • deficiency/ resistance to aldosterone bc psuedomypoaldosteronism or drug
  • low aldosterone/ failure to respond to it
  • decrease NH3 synthesis by PT
  • ACE inhibitors , spironolactone can cause this

impair acid-base homeostasis

43
Q

Metabolic Acidosis Symptoms

  • mild
  • with ph <7.10
A

mild acidosis- asymptomatic

with ph< 7.10 ( or higher if rapidly developed)
- nausea, vomiting, malaise

see long deep breaths at normal rate (respiratory compensation) without dyspnea

44
Q

Metabolic Alkalosis with Compensation and Correction

- pathway

A

Renal
- high serum ph-> decrease tubular reabsorption of bicarbonate -> increase bicarbonate excretion in urine -> low serum ph

  • high serum ph-> decrease acid titration -> decrease ammonium and HPO4-> decrease bicarbonate regeneration -> decrease acid excretion in urine -> low serum pH

Respiratory
- high serum ph-> hypoventilation -> increase PCO2-> increase CO2 + H2O-> increase H2Co3-> increase H+ -> low serum ph

45
Q

Causes of Metabolic Alkalosis (8)

A
  • Contraction
  • Licorice
  • Endo ( Conn, Cushing, Bartter)
  • Vomiting
  • Excess Alkali
  • Refeeding Alkalosis
  • Post-hypercapnia
  • Diuretics
46
Q

Causes of Metabolic Alkalosis

A

1) Loss of H (vomiting, hyperaldosteronism)
2) Gain of HCO3 (ingestion of NaHCo3)
3) Volume contraction alkalosis (loop or thiazide diuretic)

47
Q

Metabolic Alkalosis Symptoms

  • mild
  • more severe
A

Mild: symptoms of underlying disorder

severe: increased binding of CA2+=> hypocalcemia
- headache, lethargy, neuromuscular excitability,
- delirium, tetany, seizures
- angina symptoms, arrhytias, weakness

48
Q

Respiratory Acidosis with compensation

- pathway

A

decrease ventilation-> increase blood PCo2-> increase bicarbonate-> low serum ph -> renal compensation-> increased acid titration -> increase ammonium and HPO4–> increase acid excretion in urine-> increase bicarbonate regeneration-> increase serum pH

49
Q

Causes of Respiratory Acidosis

  • acute (4)
  • chronic (2)
A 
Acute
CANS
- CNS depression 
- Airway obstruction
- Neuromuscular disorders
- Sever Pneumonia, embolism, edema

Chronic

  • COPD ( chronic obstructive pulmonary disease)
  • anything chronic that leads to impaired ventilation
50
Q

Causes of Respiratory Acidosis (4)

A

1) inhibition of medullary respiratory center
- opiates, barbiturates
2) disorders of respiratory muscles
- ALS
- MS
3) airway obstruction
- aspiration
- obstructive sleep apnea
- laryngospasm
4) disorders of gas exchange
- COPD
- Pneumonia
- pulmonary edema

51
Q

Respiratory Acidosis Symptoms

  • acute
  • slowly developing, stable
A

acute
- headache, confusion, anxiety, drowsiness, stupor, tremors, convulsion, possible coma (CO2, narcosis)

Slowly developing, Stable (as in COPD)

  • may be well tolerated
  • memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes
  • gait disturbance, tremor, blunted deep tendon reflexes, myoclonic jerks, asterixis, papilledema
52
Q

Respiratory Alkalosis with Compensation

- pathway

A

increased ventilation-> low blood PCo2-> decrease H+ and H2CO3-> increase serum pH-> renal compensation-> decreased acid titration-> decrease NH4 and HPO4-> decrease acid excretion in urine-> decrease bicarbonate regeneration -> low serum ph

53
Q

Causes of Respiratory Alkalosis (6)

A

CHAMPS

  • CNS Disease
  • Hypoxia
  • Anxiety
  • Mechanical Ventilators
  • Progesterone
  • Salicylates/ Sepsis
54
Q

Causes of Respiratory Alkalosis (3)

A

1) stimulation of medullary respiratory center
- neurological disorder
2) Hypoxemia
- high altitude
- pneumonia
- pulmonary embolism
- severe anemia
3) Mechanical Ventilation

55
Q

Respiratory Alkalosis Symptoms

  • acute
  • chronic
A

Acute

  • light headedness
  • confusion
  • peripheral and circumoral paresthesias
  • cramps
  • syncope
  • tachypnea/ hyperpnea
  • carpopedal spasm due to decrease hypocalcemia

Chronic
- asymptomatic

56
Q

Metabolic Acidosis Equations

A

PaCo2= 40- (1.2 x (24-HCO3-)

PaCo2= (1.5 x HCO3) + 8 +/- 2

57
Q

Metabolic Alkalosis Equation

A

PaCo2= 40 + (0.7 x HCO3- 24)

must be less than 20

58
Q

Respiratory Acidosis Equations

A

Acute
HCO3- = 24 + (0.1 X (PaCo2-40))

Chronic
HCO3-= 24 + (0.4 X (PaCo2-40))

59
Q

Respiratory Alkalosis Equations

A

Acute
HCO3- = 24 - (0.2 X (40- PaCo2))

Chronic
HCO3-= 24 - (0.5 X (40-PaCo2))

Range +/- 2

Renal Final (7 decks)

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